47 research outputs found
Quality check of cardiac MRI exams for Fallot patients: Interest of a simple formula to detect invalid exams
PurposeCardiac MRI (CMR) is the key exam for Fallot patients but remains tricky. The CMR report should at least mention left and right ventricle end-diastole volumes (Vl and Vr), ejection fraction (EFl and EFr) and pulmonary regurgitation (PR). Obviously, these variables are linked together by basic physiology rules and indeed VlĂEFl=VrĂEFrĂ(1-PR). We investigated the interest of using such formula as quality check during Fallot CMR exams in our center.Methods98Â consecutive CMR examinations for Fallot (or Fallot-like) cardiopathy between 2010 and 2014 were retrospectively included. The exams failing to pass the formula (with a 10% tolerance) constituted the Invalid-group and a control group of the same size was also constituted. CMR of both groups were randomly submitted to a blinded senior observer. The inter-observer limits of agreements were compared for the different variables within both groups.Results(Fig. 1) 12Â CMR (12%) failed to pass the validation formula. From the 24 reanalyzed CMR, only 4 failed to pass the formula (all from the Invalid-group). Two had persistent defect (VSD or ASD) which were not mentioned to the radiologist and not detected during the CMR. Two had significant artefacts in the aorta or pulmonary trunk due to sterna wires. The inter-observer disagreements for the 8 other CMR of the Invalid-group concerned the Right ventricle end-diastole volume (P<0.05).ConclusionThe use of a simple formula as quality check of CMR examinations for Fallot patients was useful to detect a total of 12% of CMR with issues. 8% of the CMR corresponded to uncertain right ventricle contours, 2% to persistent septal defects that should have been noticed during the examination and 2% to unreliable aortic or pulmonary flow due to artifacts. The formula could have permitted either to detect the anomalies or at least to conclude that the quality of the exams was impaired
Fast assessment of long axis strain with standard cardiovascular magnetic resonance: a validation study of a novel parameter with reference values
Background: Assessment of longitudinal function with cardiovascular magnetic resonance (CMR) is limited to measurement of systolic excursion of the mitral annulus (MAPSE) or elaborate strain imaging modalities. The aim of this study was to develop a fast assessable parameter for the measurement of long axis strain (LAS) with CMR. Methods: 40 healthy volunteers and 125 patients with different forms of cardiomyopathy were retrospectively analyzed. Four different approaches for the assessment of LAS with CMR measuring the distance between the LV apex and a line connecting the origins of the mitral valve leaflets in enddiastole and endsystole were evaluated. Values for LAS were calculated according to the strain formula. Results: LAS derived from the distance of the epicardial apical border to the midpoint of the line connecting the mitral valve insertion points (LAS-epi/mid) proved to be the most reliable parameter for the assessment of LAS among the different approaches. LAS-epi/mid displayed the highest sensitivity (81.6 %) and specificity (97.5 %), furthermore showing the best correlation with feature tracking (FTI) derived transmural longitudinal strain (râ=â0.85). Moreover, LAS-epi/mid was non-inferior to FTI in discriminating controls from patients (Area under the curve (AUC)â=â0.95 vs. 0.94, pâ=âNS). The time required for analysis of LAS-epi/mid was significantly shorter than for FTI (67â±â8 s vs. 180â±â14 s, pâ<â0.0001). Additionally, LAS-epi/mid performed significantly better than MAPSE (Delta AUCâ=â0.09; pâ<â0.005) and the ejection fraction (Delta AUCâ=â0.11; pâ=â0.0002). Reference values were derived from 234 selected healthy volunteers. Mean value for LAS-epi/mid was â17.1â±â2.3 %. Mean values for men were significantly lower compared to women (â16.5â±â2.2 vs. -17.9â±â2.1 %; pâ<â0.0001), while LAS decreased with age. Conclusions: LAS-epi/mid is a novel and fast assessable parameter for the analysis of global longitudinal function with non-inferiority compared to transmural longitudinal strain
Tectonic structure, evolution, and the nature of oceanic core complexes and their detachment fault zones (13°20âČN and 13°30âČN, Mid Atlantic Ridge)
Microbathymetry data, in situ observations, and sampling along the 138200N and 138200N oceanic
core complexes (OCCs) reveal mechanisms of detachment fault denudation at the seafloor, links between tectonic
extension and mass wasting, and expose the nature of corrugations, ubiquitous at OCCs. In the initial
stages of detachment faulting and high-angle fault, scarps show extensive mass wasting that reduces their
slope. Flexural rotation further lowers scarp slope, hinders mass wasting, resulting in morphologically complex
chaotic terrain between the breakaway and the denuded corrugated surface. Extension and drag along the fault
plane uplifts a wedge of hangingwall material (apron). The detachment surface emerges along a continuous
moat that sheds rocks and covers it with unconsolidated rubble, while local slumping emplaces rubble ridges
overlying corrugations. The detachment fault zone is a set of anostomosed slip planes, elongated in the alongextension
direction. Slip planes bind fault rock bodies defining the corrugations observed in microbathymetry
and sonar. Fault planes with extension-parallel stria are exposed along corrugation flanks, where the rubble cover
is shed. Detachment fault rocks are primarily basalt fault breccia at 138200N OCC, and gabbro and peridotite
at 138300N, demonstrating that brittle strain localization in shallow lithosphere form corrugations, regardless of
lithologies in the detachment zone. Finally, faulting and volcanism dismember the 138300N OCC, with widespread
present and past hydrothermal activity (Semenov fields), while the Irinovskoe hydrothermal field at the
138200N core complex suggests a magmatic source within the footwall. These results confirm the ubiquitous
relationship between hydrothermal activity and oceanic detachment formation and evolution
Fast assessment of long axis strain with standard cardiovascular magnetic resonance: a validation study of a novel parameter with reference values
Quality check of cardiac MRI exams for Fallot patients: Interest of a simple formula to detect invalid exams
Effects of selective inhibitors of Aurora kinases on anaplastic thyroid carcinoma cell lines
Aurora kinases are serine/threonine kinases that play an essential role in cell division. Their aberrant expression and/or function induce severe mitotic abnormalities, resulting in either cell death or aneuploidy. Overexpression of Aurora kinases is often found in several malignancies, among which is anaplastic thyroid carcinoma (ATC). We have previously demonstrated the in vitro efficacy of Aurora kinase inhibitors in restraining cell growth and survival of different ATC cell lines. In this study, we sought to establish which Aurora might represent the preferential drug target for ATC. To this end, the effects of two selective inhibitors of Aurora-A (MLN8237) and Aurora-B (AZD1152) on four human ATC cell lines (CAL-62, BHT-101, 8305C, and 8505C) were analysed. Both inhibitors reduced cell proliferation in a time- and dose-dependent manner, with IC50 ranges of 44.3-134.2ânM for MLN8237 and of 9.2-461.3ânM for AZD1152. Immunofluorescence experiments and time-lapse videomicroscopy yielded evidence that each inhibitor induced distinct mitotic phenotypes, but both of them prevented the completion of cytokinesis. As a result, poliploidy increased in all AZD1152-treated cells, and in two out of four cell lines treated with MLN8237. Apoptosis was induced in all the cells by MLN8237, and in BHT-101, 8305C, and 8505C by AZD1152, while CAL-62 exposed to AZD1152 died through necrosis after multiple rounds of endoreplication. Both inhibitors were capable of blocking anchorage-independent cell growth. In conclusion, we demonstrated that either Aurora-A or Aurora-B might represent therapeutic targets for the ATC treatment, but inhibition of Aurora-A appears more effective for suppressing ATC cell proliferation and for inducing the apoptotic pathway